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Hormonal changes following tumor transplantation: Factors increasing corticosterone and the relationship of corticosterone to tumor‐induced anti‐inflammation
Author(s) -
Normann S.,
Besedovsky H.,
Schardt M.,
Del Rey A.
Publication year - 1988
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910410613
Subject(s) - corticosterone , endocrinology , medicine , transplantation , adrenalectomy , inflammation , ascites , hormone
Abstract EL‐4 lymphoma cells transplanted to syngeneic C57BL/6J mice induced a biphasic decrease in inflammation and a biphasic increase in serum levels of corticosterone. In addition, this tumor altered serum levels of 3 other hormones, resulting in a biphasic decrease in insulin, an early decrease in protactin, and a terminal severe deficiency in thyroxine. Early changes occurred 16 to 48 hr after tumor transplantation and were of variable duration, while late‐phase defects developed during the last few days of life. Soluble factors associated with tumor growth may mediate certain hormonal changes since serum levels of corticosterone increased and insulin decreased following injection of tumorous ascites into normal mice. Further, injection of cell‐free tumor culture supernatants increased corticosterone levels. Hormonal changes following injection of soluble factors occurred after a delay of 16 hr indicating that the factors acted indirectly. Surgical adrenalectomy blocked the corticosterone increase induced by tumor transplantation or ascites injection and eliminated the anti‐inflammatory effect of tumor transplantation while significantly decreasing the effect associated with injection of tumorous ascites. Thus, the physiologically induced increase in serum levels of corticosterone reached anti‐inflammatory levels. Further, elevated levels of corticosterone are a major contributing factor to anti‐inflammation induced by tumorous ascites injection and constitute the principal mechanism of anti‐inflammation following tumor transplantation.